Research progress on the relationship between Fusobacterium nucleatum and periodontitis / 口腔疾病防治

@#Periodontitis is an infectious disease caused by a variety of microorganisms. Fusobacterium nucleatum is closely related to periodontitis with a high detection rate. Fusobacterium nucleatum is able to coaggregate with other microorganisms and attach and invade epithelial cells with the help of adhesins. It can also promote the occurrence and development of periodontal diseases and even systemic diseases by destroying periodontal tissues with virulence factors and metabolites and inducing a host immune response. However, at present, drugs assisting periodontal nonsurgical treatment clinically cannot target specific periodontal pathogens, such as Fusobacterium nucleatum, which may lead to problems such as dysbacteriosis or drug resistance. Therefore, studies on the pathogenic mechanism of Fusobacterium nucleatum provide new ideas for the prevention and treatment of periodontitis. The idea is to develop materials, drugs, or probiotics that target adhesins, virulence factors, and metabolites or cut off each pathogenic pathway of Fusobacterium nucleatum to inhibit its proliferation and inflammatory responses in deep periodontal pockets and achieve a balance with other oral microorganisms, and the host is beneficial for the control of periodontitis.

Cytokine Production in Cholangiocarcinoma Cells in Response to Clonorchis sinensis Excretory-Secretory Products and Their Putative Protein Components

Clonorchis sinensis is a carcinogenic human liver fluke that promotes hepatic inflammatory environments via direct contact or through their excretory-secretory products (ESPs), subsequently leading to cholangitis, periductal fibrosis, liver cirrhosis, and even cholangiocarcinoma (CCA). This study was conducted to examine the host inflammatory responses to C. sinensis ESPs and their putative protein components selected from C. sinensis expressed sequenced tag (EST) pool databases, including TGF-β receptor interacting protein 1(CsTRIP1), legumain (CsLeg), and growth factor binding protein 2 (CsGrb2). Treatment of CCA cells (HuCCT1) with the ESPs or bacterial recombinant C. sinensis proteins differentially promoted the secretion of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) as well as anti-inflammatory cytokines (IL-10, TGF-β1, and TGF-β2) in a time-dependent manner. In particular, recombinant C. sinensis protein treatment resulted in increase (at maximum) of ~7-fold in TGF-β1, ~30-fold in TGF-β2, and ~3-fold in TNF-α compared with the increase produced by ESPs, indicating that CsTrip1, CsLeg, and CsGrb2 function as strong inducers for secretion of these cytokines in host cells. These results suggest that C. sinensis ESPs contribute to the immunopathological response in host cells, leading to clonorchiasis-associated hepatobiliary abnormalities of greater severity.

Serum antibody & Th2 cytokine profiles in patients with cystic echinococcosis.

Background & objectives: Human cystic echinococcosis (CE), caused by Echinococcus granulosus, is one of the most important and widespread parasitic zoonoses. T helper cell-2 (Th2) dominated immunity in CE is associated with increased susceptibility to the disease, while T helper cell-1 (Th1) cell activation is assumed to induce protective immunity. Hence, in order to investigate in vivo Th2 cell activation and serum complement levels, the present study was aimed to detect serum levels of specific IgG, IgE, interleukin (IL)-4, IL-10, C3c and C4 in confirmed CE patients. Methods: Specific IgG levels in serum was measured by enzyme linked immunosorbent assay using recombinant E. granulosus antigen-B/2 (RecEg-AgB/2) and serum IgE, IL-4, IL-10, C3c and C4 were quantified by nephelometry in 45 surgically confirmed patients with CE, and 10 healthy controls. Results: Specific IgG (P<0.0001), IgE (P<0.05), IL-4 (P=0.0197) and IL-10 (P<0.01) levels were significantly elevated in CE cases compared to healthy controls. IL-4 could be detected in 34 patients (75.55%) and six controls (60%) in a low concentration. The IgE concentration was elevated (>120 U/ml) in 36 (80%) cases of CE and in one healthy control. Interpretation & conclusion: Our results showed higher C3c and C4 levels in CE patients than healthy controls. No significant association was found between IgE concentrations and cytokine levels. The results of this study point to a cytokine profile suggestive of Th2 cell dominance in vivo in CE.

The Effect of Iron Depletion on the Monocytic Adhesion, Differentiation and SR-A Expression / 대한해부학회지

Maintenance of cellular iron homeostasis is a prerequisite for proliferation and differentiation of cells, and is also a central role in the regulation of immune function. Monocyte-macrophages play an important roles in host defense, particularly in the inflammatory process of acute and chronic disease. The reason that an iron is important in these cell is because an iron is indispensable in a generation of hydroxyl radical for bacterium killing. Because of the role of iron in the monocytic THP-1 cell differentiation is not become clear, we investigated whether THP-1 cell can differentiate to macrophage-like cell using of iron and iron chelator which cause iron depletion. The cell differentiation was not able to observe by iron treatment, by the way, the cell adhesion was increased in DFO treated monocyte and cellular pseodopodial extension, change of a nucleus-cytoplasmic ratio were showed in Differential interference contrast (DIC) and Giemsa staining, and it was inhibited by ferric citrate (FC). Increased polystyrene bead phagocytosis by DFO treatment of THP-1 cell were detected through FACS and rhodamine-phallodin staining. The SR-A expression, which was a cell differentiation marker, was increased by DFO treatment of THP-1 cell. These results suggest that iron depletion by DFO can promote THP-1 cell diffentiation into macrophage-like cell, and this may carrying out important role in the immune response.